Another pivotal component of systemic iron homeostasis is hepcidin, a circulating peptide hormone synthesized by hepatocytes in iron loading conditions and secreted in plasma and urine. Hepcidin regulates the entry of iron into plasma through ferroportin. Hepcidin, by binding to ferroportin, causes ferroportin phosphorylation, internalization and degradation in lysosomes, thus hindering iron export and enhancing cytosolic iron storage in ferritin. Iron homeostasis disorders appear to arise from hepcidin and/or ferroportin dysregulation. Similarly to the regulation of maternal systemic iron homeostasis, fetal hepcidin controls the transfer of maternal iron across the placenta to the fetus and the enhanced placental-fetal iron transport is related to an increased expression of ferroportin on placental basal fetal-facing membrane, consistent with unidirectional mother-fetus iron transport. Even if the interaction of hepcidin with ferroportin can explain the regulation of iron homeostasis at systemic level, the influence of iron metabolism on critical stage of fetal development, is still unknown.